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Catecholamine Response to Exercise in Obese, and Lean Boys

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Catecholamine Response to Exercise in Obese, and Lean Boys

Abstract and Introduction

Abstract


Introduction: The aim of this study was to examine the effect of body fat percentage on the plasma catecholamine response to a cycling sprint test (CST) in sedentary adolescent boys.
Methods: In this study, 31 adolescent boys (9 obese (% body fat = 31.0% ± 3.0%), 11 overweight (% body fat = 24.0% ± 1.6%), and 11 lean (% body fat = 16.0% ± 1.9%)), matched for peak oxygen consumption, completed a CST consisting of six 6-s maximal sprints with 2 min of passive rest between each repetition. Performance of each subject was determined as the mean power output (POmean) developed during the CST. Plasma lactate, epinephrine, and norepinephrine concentrations were determined successively at rest, after a 10-min warm-up, immediately after the CST, and after 20 min of passive recovery.
Results: Although groups were not different in age, height, or peak oxygen consumption (mL kg fat-free mass min), maximal epinephrine concentration was significantly (P < 0.05) higher in lean vs obese and was negatively correlated to body fat percentage (r = –0.60, P < 0.05). Maximal norepinephrine values were higher in lean versus overweight and obese, and a negative relationship was found between maximal norepinephrine concentration and body fat percentage (r = –0.60, P < 0.05). Maximal lactate concentration was higher in lean versus overweight and obese (14.7 ± 3.3, 10.4 ± 2.7, and 10.2 ± 2.5 mM in lean, overweight, and obese, respectively). A significant relationship was also obtained between maximal norepinephrine and maximal epinephrine values with both maximal lactate concentration (r = 0.60 and r = 0.60, P < 0.05, respectively) and POmean (r = 0.65 and r = 0.6, P < 0.05).
Conclusions: Our results show that the catecholamine response to a CST was affected by body fat percentage, with reduced epinephrine and norepinephrine values in overweight and obese adolescents.

Introduction


Childhood obesity is a major, uncontrolled worldwide epidemic with serious psychosocial and medical consequences due to comorbidities such as early-onset dyslipidemia, hypertension, and insulin resistance. Childhood obesity is also considered a key predictor for obesity in adulthood. Obesity treatment programs rely on dietary changes combined with regular exercise for successful weight loss. The ability to mobilize adipose tissue fat for oxidization in muscle during exercise is important to the success of an exercise training–related weight loss program. Catecholamines are known to play a major role in the regulation of intermediary metabolism, affecting glucose production, muscle glycogen mobilization, and lipolysis, all of which affect exercise metabolism and performance. Reductions in the catecholamine response to exercise could disrupt fat mobilization and oxidation, preventing the desired loss of adipose in overweight or obese individuals.

Human studies indicate that obese and overweight individuals have altered hormone responses both at rest and in response to stimuli such as hypoglycemia or exercise. Obese individuals have been shown to exhibit significantly reduced growth hormone and catecholamine responses during exercise. Whether the altered hormonal response is the result of or contributes to the cause of obesity is uncertain. The majority of the studies examining the effect of obesity on exercise-associated hormonal responses have been conducted on adults. There is little information on the effects of obesity on the catecholamine response at rest and during exercise in adolescents. Eliakim et al. observed a blunted catecholamine response to exercise in obese compared with lean adolescents (girls and boys were combined). The exercise consisted of ten 2-min bouts of constant-cycle ergometer above anaerobic threshold, with 1 min of rest between each bout. More recently, Zouhal et al. observed no significant differences in plasma epinephrine and norepinephrine concentrations between obese and nonobese adolescent girls in response to a maximal incremental exercise test. These divergences may, at least in part, be explained by methodological differences between these studies such as gender, exercise protocol, or exercise intensity.

For lean subjects, catecholamine responses may influence performance during high-intensity exercise by controlling muscular and hepatic glycogenolysis. However, the role of catecholamines is less clear in the obese population. Exercise performance, assessed by a stairs climbing test or using the force–velocity test (F/V ), was significantly lower compared with nonobese subjects. The difference in performance was thought to be related to the excess fat mass in obese population. Considering that hormonal factors, especially catecholamines, play a considerable role in exercise performance, it is possible that a difference in the plasma catecholamine response to exercise in overweight or obese individuals could influence exercise performance.

We know of no studies that have examined the catecholamine response to exercise in adolescent boys with varying levels of fat mass. Therefore, the purpose of this study was to determine whether fat mass affects exercise performance and the catecholamine responses to a repeat cycling sprint test (CST) in overweight, obese, and lean adolescent boys.

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